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Citral exerts its antifungal activity against Penicillium digitatum by affecting the mitochondrial morphology and
Shiju Zheng1, Guoxing Jing1, Xiao Wang1
1School of Chemical Engineering, Xiangtan University, Xiangtan 411105, PR China.
Abstract:
This work investigated the effect of citral on the mitochondrial morphology and function of Penicillium digitatum. Citral at concentrations of 2.0 or 4.0 μL/mL strongly damaged mitochondria of test pathogen by causing the loss of matrix and increase of irregular mitochondria. The deformation extent of the mitochondria of P. digitatum enhanced with increasing concentrations of citral, as evidenced by a decrease in intracellular ATP content and an increase in extracellular ATP content of P. digitatum cells. Oxygen consumption showed that citral resulted in an inhibition in the tricarboxylic acid cycle (TCA) pathway of P. digitatum cells, induced a decrease in activities of citrate synthetase, isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinodehydrogenase and the content of citric acid, while enhancing the activity of malic dehydrogenase in P. digitatum cells. Our present results indicated that citral could damage the mitochondrial membrane permeability and disrupt the TCA pathway of P. digitatum.
Insights
Citral damages Penicillium digitatum mitochondria and disrupts its tricarboxylic acid cycle (TCA) pathway. This antifungal activity increases with higher citral concentrations, impacting energy production and cell integrity.
Area of Science:
- Mycology
- Biochemistry
- Plant Pathology
Background:
- Penicillium digitatum is a significant post-harvest pathogen affecting citrus fruits.
- Mitochondrial function is crucial for fungal cell viability and pathogenesis.
- Citral, a natural monoterpene aldehyde, exhibits antimicrobial properties.
Purpose of the Study:
- To investigate the effects of citral on the mitochondrial morphology and function of Penicillium digitatum.
- To elucidate the mechanism underlying citral's antifungal activity against this pathogen.
Main Methods:
- Exposure of Penicillium digitatum to varying concentrations of citral (2.0 and 4.0 μL/mL).
- Microscopic examination of mitochondrial morphology.
- Measurement of intracellular and extracellular ATP content.
- Assessment of oxygen consumption and key enzyme activities within the tricarboxylic acid (TCA) cycle.
Main Results:
- Citral caused significant mitochondrial damage, including matrix loss and increased irregularity, in a dose-dependent manner.
- Intracellular ATP levels decreased while extracellular ATP levels increased, indicating compromised cell membrane integrity.
- Citral inhibited the TCA pathway by reducing the activities of citrate synthetase, isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, and succinate dehydrogenase, and decreasing citric acid content.
- Malate dehydrogenase activity was enhanced, suggesting a metabolic shift.
Conclusions:
- Citral disrupts mitochondrial membrane permeability in Penicillium digitatum.
- Citral effectively inhibits the tricarboxylic acid (TCA) cycle, leading to impaired energy metabolism and fungal growth.
- These findings highlight citral as a potential agent for controlling Penicillium digitatum infections.
